PMID- 8874623 OWN - NLM STAT- MEDLINE DCOM- 19970116 LR - 20111117 IS - 0269-9370 (Print) IS - 0269-9370 (Linking) VI - 10 IP - 10 DP - 1996 Sep TI - Identification of multiple HIV-1 cytotoxic T-cell epitopes presented by human leukocyte antigen B35 molecules. PG - 1075-83 AB - OBJECTIVE: To identify HIV-1 cytotoxic T lymphocyte (CTL) epitopes presented by human leukocyte antigen (HLA)-B35 molecules that are associated with the accelerated progression of AIDS using a reverse immunogenetic approach. METHODS: 8-mer to 11-mer sequences carrying two anchor residues at position 2 and the carboxy-terminus were selected from HIV-1SF2 strain. Sixty-four peptides matched to these sequences were synthesized and tested by a peptide binding assay using RMA-S-B*3501 cells. Peripheral blood lymphocytes (PBL) from two HIV-1-infected donors carrying HLA-B35 were stimulated once-weekly with each HLA-B*3501 binding peptide. The CTL activity of the cultured cells for the HLA-B35-positive target cells loaded with the corresponding peptides was examined after the second and fourth stimulation. Furthermore, the CTL activity of the cultured cells possessing HLA-B*3501-restricted HIV-1 peptide-specific CTL activity were examined for the HLA-B*3501-positive target cells infected with the recombinant vaccinia virus containing corresponding HIV-1 gene. RESULTS: HIV-1 peptide-specific HLA-B*3501-restricted CTL was induced in PBL of HIV-1 infected donors by in vitro stimulation with 11 out of 27 HLA-B*3501-binding HIV-1 peptides. The specific CTL induced with 10 peptides killed the cells infected with recombinant vaccinia virus expressing the corresponding HIV-1 proteins. Out of these HIV-1 peptide epitopes, two epitopes were also presented by HLA-B51 molecules. CONCLUSION: In addition to the four HLA-B35-restricted HIV-1 CTL epitopes that have been previously reported, nine HLA-B35-restricted HIV-1 CTL epitopes were identified in the present study. These multiple epitopes will be useful in studies for immunopathogenesis of AIDS. FAU - Shiga, H AU - Shiga H AD - Institute of Medical Science, University of Tokyo, Japan. FAU - Shioda, T AU - Shioda T FAU - Tomiyama, H AU - Tomiyama H FAU - Takamiya, Y AU - Takamiya Y FAU - Oka, S AU - Oka S FAU - Kimura, S AU - Kimura S FAU - Yamaguchi, Y AU - Yamaguchi Y FAU - Gojoubori, T AU - Gojoubori T FAU - Rammensee, H G AU - Rammensee HG FAU - Miwa, K AU - Miwa K FAU - Takiguchi, M AU - Takiguchi M LA - eng PT - Comparative Study PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - AIDS JT - AIDS (London, England) JID - 8710219 RN - 0 (Epitopes) RN - 0 (HLA-B Antigens) RN - 0 (HLA-B35 Antigen) RN - 0 (HLA-B51 Antigen) RN - 0 (Oligopeptides) RN - 0 (Recombinant Proteins) SB - IM MH - *Antigen Presentation MH - *Cytotoxicity, Immunologic MH - *Epitopes MH - HIV-1/genetics/*immunology MH - HLA-B Antigens/immunology MH - HLA-B35 Antigen/*immunology MH - HLA-B51 Antigen MH - Humans MH - Mutation MH - Oligopeptides/genetics/immunology/metabolism MH - Protein Binding MH - Recombinant Proteins/immunology MH - T-Lymphocytes/*immunology MH - Vaccinia virus/genetics EDAT- 1996/09/01 00:00 MHDA- 1996/09/01 00:01 CRDT- 1996/09/01 00:00 PHST- 1996/09/01 00:00 [pubmed] PHST- 1996/09/01 00:01 [medline] PHST- 1996/09/01 00:00 [entrez] PST - ppublish SO - AIDS. 1996 Sep;10(10):1075-83.